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News from corporate.dukemedicine.orgen-usTue, 03 Mar 2015 19:08:42 -0500Tue, 03 Mar 2015 19:08:42 -0500http://blogs.law.harvard.edu/tech/rssCopyright (c)2004-2015 Duke University Health System1440corporate.dukemedicine.org: Duke Medicine News14026http://corporate.dukemedicine.org/news_and_publications/news_office/news?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/images/dukemedicine_rss.pnghttp://corporate.dukemedicine.org/news_and_publications/news_office/news/investigational-therapy-could-attack-cause-of-sickle-cell-crises?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/investigational-therapy-could-attack-cause-of-sickle-cell-crises<p>DURHAM, N.C. – Treatment for painful episodes of blood vessel obstruction in sickle cell anemia is currently limited to controlling pain, but an investigational therapy might be able to interfere with the underlying cause of these events, known as vaso-occlusion crises, researchers at Duke Medicine report.</p>
<div>In a small, multicenter patient study led by Marilyn J. Telen, M.D., Wellcome Professor of Medicine in the division of hematology at Duke University Medical School, patients who received an investigational drug had quicker resolution of the pain episode, although the difference compared to a control group did not rise to statistical significance.</div>
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<div>Telen said the study’s small size, as well as the wide variability in the length of time that all of the study patients suffered painful vascular obstruction, contributed to the statistical draw. A larger, international study is planned to begin later this year to provide greater clarity.</div>
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<div>Patients who received the investigational drug also used far less pain medication, which was self-administered. Those findings were statistically significant.</div>
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<div>The findings were reported online March 2, 2015, in the journal <a href="http://app.bronto.com/public/?q=ulink&amp;fn=Link&amp;ssid=9780&amp;id=gva7zpstj89d6o25utukgiua8k6q9&amp;id2=ee5mxdvwfcq37q2gsz8ehcnaqu1h3&amp;subscriber_id=bfwvmoyadeyrcvdzippdwillbpcpben&amp;delivery_id=bshvmnemjtpepurspbxvgebmuiqhbdm&amp;tid=3.JjQ.B9742Q.D56K.AaO8SA..AgSTtQ.b..l.Ak87.a.VPUccg.VPUc8A.IQcvgw" target="_blank">Blood</a>.</div>
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<div>“We have not had good therapies for people with this disease,” Telen said. “But this approach shows more promise than anything else I’ve seen in 34 years of treating sickle cell disease.”</div>
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<div>Sickle cell anemia is a genetic condition in which some of the red blood cells are stiff and shaped like crescents, or sickles, rather than smooth and round. The abnormal blood cells can build up and block blood flow to limbs and organs, causing severe pain and organ damage. </div>
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<div>The National Heart, Lung, and Blood Institute estimates that up to 100,000 people in the United States, primarily African-Americans, have the disease. The disease affects millions of people throughout the world, and causes more than 75,000 hospitalizations a year in the United States, which accounts for $1 billion in annual U.S. medical costs.</div>
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<div>Telen said the current standard of care is pain control, typically with opioids, and patients can be hospitalized for days or weeks. Enrolling 76 patients from 17 sites in the United States, the study randomly assigned patients to receive either a placebo or the investigational drug, dubbed GMI-1070, or rivipansel. All patients also received the standard treatment for pain and symptom management.</div>
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<div>The drug is designed to prevent cells from sticking together and thereby improve blood flow. For study participants who received the investigational drug, the effects tended to begin within 24 hours, and their painful crisis passed sooner than those receiving only treatment for pain, but the statistical difference was not significant. </div>
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<div>The researchers said the improvements seen in the amount of time to resolution would likely be clinically meaningful if they were verified in a larger trial. </div>
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<div>Study authors also said the findings demonstrating lower use of pain medication among patients was a critical step forward.</div>
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<div>“The difference in pain medication use was statistically significant, and it occurred in the first 24 hours, which implies that the therapy may be interfering with the mechanism of the vaso-occlusion,” Telen said. “For these patients, having less pain is very important.”</div>
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<div>Telen said the larger study is planned to begin later this year, with a goal of enrolling more than 300 patients. </div>
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<div>In addition to Telen, study authors include Ted Wun, Timothy L. McCavit, Laura M. De Castro, Lakshmanan Krishnamurti, Sophie Lanzkron, Lewis L. Hsu, Wally R. Smith, Seungshin Rhee, John L. Magnani, and Helen Thackray.</div>
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<div>The drug developer, GlycoMimetics, Inc., funded the study. Telen has received consulting fees from the company. Full conflict disclosures are provided in the publication.</div>
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<div style="text-align: center;">###</div>Duke MedicineMon, 02 Mar 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/guidelines-suggest-blood-thinners-for-more-women-seniors?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/guidelines-suggest-blood-thinners-for-more-women-seniors<p><span style="line-height: 1.2em;">DURHAM, N.C. -- </span>Nearly all women and people over 65 in the U.S. with atrial fibrillation are advised to take blood thinners under new guidelines based on an analysis from the Duke Clinical Research Institute.</p>
<p><span>Atrial fibrillation, or AFib, is an irregular heartbeat that can lead to blood clots, stroke, heart failure and other heart-related complications. It affects about 2.7 million people in the U.S. Anticoagulant drugs help prevent blood from clotting and potentially causing stroke.</span></p>
<p><span>In 2014, the American Heart Association, American College of Cardiology and Heart Rhythm Society issued broader guidelines for the use of anticoagulants in treating AFib. Notably, being female is now included in the guidelines as a contributing risk factor for stroke, said Emily O’Brien, Ph.D., lead author of the Duke study.</span></p>
<p><span>Analysts at DCRI reviewed data from a registry called ORBIT that included 10,132 AFib patients from 176 sites across the U.S. They examined patients’ age, gender and other risk factors such as prior congestive heart failure, high blood pressure, diabetes and prior stroke. The analysis, published in JAMA-Internal Medicine, provides a roadmap for how the broader guidelines could impact the number of patients recommended for drug therapy.</span></p>
<p><span>The researchers report that the overall proportion of AFib patients recommended for blood-thinning drugs would increase by 19 percent as a result of the new guidelines, from about 72 percent of all AFib patients to 91 percent.</span></p>
<p><span>A similar increase was predicted for women with the heart condition. Under previous guidelines, about 77 percent of female AFib patients in the study population would have been recommended for treatment with anticoagulants. Under the new guidelines, 98 percent of women in the sample population would have enough risk factors to be recommended for treatment.</span></p>
<p><span>The new recommendations also lower the age at which patients are considered at risk for stroke from 75 to 65. In the study population, this meant that almost 99 percent of patients with AFib over age 65 could now be recommended for blood thinners, as compared with roughly 80 percent whose stroke risk was severe enough under the previous criteria to suggest drug therapy.</span></p>
<p><span>“The full adoption of the guidelines could reclassify nearly 1 million people with AFib who previously weren’t recommended for treatment with blood thinners,” O’Brien said. “What we don’t know yet is the extent to which doctors in community practice will incorporate the guidelines into their clinical routines, and what that will mean for the long-term outcomes for those patients. That will be the next step for our study.”</span></p>
<p><span>Patients with AFib should be confident that the new guidelines are evidence-based, but they are just one factor that a physician should consider when planning their treatment, O’Brien said. Doctors should also weigh the possible risks and benefits of drug treatment, as well as the patient’s goals and values, she said.</span></p>
<p><span>Blood thinners can protect patients against a blood clot or stroke, but might also put patients at some increased risk for bleeding. However, for most patients, the benefits outweigh the bleeding risk, O'Brien said.</span></p>
<p><span>In addition to O’Brien, study authors include Sunghee Kim; Paul L. Hess; Peter R. Kowey; Gregg C. Fonarow; Jonathan P. Piccini; and Eric D. Peterson.</span></p>
<p><span>The researchers received funding from Janssen Scientific Affairs, which markets anticoagulant therapies. The Agency of Healthcare Research and Quality provided additional support (1U19 HS021092).</span></p>
<p align="center"><span>###</span></p>Duke MedicineMon, 02 Mar 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/retinal-swelling-in-premature-infants-tied-to-poorer-neuro-development?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/retinal-swelling-in-premature-infants-tied-to-poorer-neuro-development<p>DURHAM, N.C. – Using a portable, non-invasive imaging device, a team of Duke Medicine doctors have identified swelling in the back of the eyes of premature infants that correlates with poorer neurodevelopment as the babies grow.</p>
<p>The Duke team, which pioneered the use of the hand-held tool in infants, determined that almost half of the premature babies screened had swelling in the macula region of the retina, which is responsible for central vision. </p>
<p>After two years of follow-up study, the researchers found that the infants with retinal swelling shortly after birth later had significantly lower language and motor scores on a standard developmental test.</p>
<p>The findings, published in the March, 2015, issue of the journal Ophthalmology, suggest that the screening tool could flag potential neuro-developmental issues early, providing opportunities to intervene. </p>
<p>“The eyes are a direct window into the brain,” said senior author Cynthia Toth, M.D., a pediatric retinal specialist at the Duke Eye Center. “For the first time, we can identify microscopic swelling of the retina through a simple examination at the bedside. Because the retina is actually an extension of brain tissue, we wondered if this swelling might reflect events in ongoing brain development.”</p>
<p>Toth and colleagues used a portable cart with a handheld tool called a spectral-domain optical coherence tomography, which was originally adapted for pediatric use through research at Duke supported by the National Institutes of Health and by The Hartwell Foundation.</p>
<p>The hand-held “camera head” is similar in size to a small hair dryer, and is aimed into but does not touch the infant’s eyes. It uses infrared light that does not cause discomfort. The device enables the ophthalmologists to clearly see the cell layers at the back of the eye.</p>
<p>Of 77 premature infants born at Duke University Hospital and screened with the device, 53 were later evaluated by Kathryn Gustafson, Ph.D., at between 18 and 24 months using the Bayley Scales of Infant and Toddler Development, which measures cognitive, language and motor function. </p>
<p>Twenty-two of the children who were followed over time did not have the retinal swelling as infants, while 31 did.</p>
<p>At the 24-month evaluation, the mean score for children who had swelling was about 14 points lower on the language scale, and 11.5 points lower on the motor scale. Although infants with retinal swelling also scored lower on the cognitive scale, the difference was not significant. </p>
<p>Differences were maintained after adjusting for gestational age and birth weight. Severity of retinal swelling correlated with poorer motor development.</p>
<p>“No one knows the cause of this swelling in infants,” said first author Adam L. Rothman. “Now that we have this pilot data, it suggests that a mechanism related to poorer neurologic health may cause the retinal finding. The hope is that in the future we will be able to go into a nursery, image these babies’ eyes, and identify red flags for poor neurologic health and development. Clearly, further studies are needed to verify these findings and develop methods to use these data to improve infant care.”</p>
<p>Toth and Rothman said the current study would continue to monitor the children over time, and in future studies they will look with greater detail at eye and brain development. </p>
<p>In addition to Toth, Gustafson and Rothman, study authors include Du Tran-Viet, Ricki F. Goldstein, Maureen G. Maguire, Vincent Tai, Neeru Sarin, Amy Y. Tong, Jiayan Huang, Laura Kupper, Michael Cotten and Sharon F. Freedman.</p>
<p>The study received funding in part from the National Institutes of Health Roadmap for Medical Research (1UL1RR024128-01) and the National Eye Institute (P30 EY001583).</p>
<p align="center">###</p>Duke MedicineTue, 24 Feb 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-awarded-10-4-million-contract-to-continue-developing-radiation-test?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-awarded-10-4-million-contract-to-continue-developing-radiation-test<p>DURHAM, N.C. – In the event of nuclear meltdown or improvised nuclear bomb, presumed victims of radiation exposure would overwhelm emergency responders and hospitals. Victims can’t smell or see radiation around them, and low-level exposure doesn’t result in obvious bodily injury. The likely outcome: long lines of patients with no visual symptoms, panicked and difficult to assess.</p>
<p><span xml="lang">Duke University researchers are developing a blood test that can tell in just hours how much radiation a person has absorbed from a nuclear incident. During a large-scale emergency such as the meltdown at the Japanese Fukushima Daiichi reactors in 2011, faster testing could give doctors and patients clarity about the extent of exposures and which victims need medical care.</span></p>
<p><span xml="lang">This month, the Biomedical Advanced Research and Development Authority (BARDA), a division of the U.S. Department of Health and Human Services, awarded Duke an additional $10.4 million contract to continue the program through early 2016, bringing total funding since 2009 to more than $43 million.</span></p>
<p><span xml="lang">The multi-gene test, called a biodosimeter, comprises the work of scientists under the leadership of Dr. Nelson Chao, M.D., M.B.A., at Duke University; Dr. Frederic Zenhausern, Ph.D., M.B.A., at the University of Arizona; and scientists at Thermo Fisher Scientific and DxTerity Diagnostics. DxTerity representatives said they expect to take the biodosimeter to the Food and Drug Administration for approved medical use within the next three years.</span></p>
<p><span xml="lang">The project builds on almost a decade of study at Duke of the human response to ionizing radiation, said Gary Phillips, Duke’s BARDA program manager.</span></p>
<p><span xml="lang">The key to the test lies in a gene signature that indicates radiation absorption in the body. Researchers Dr. Holly Dressman, Ph.D., Dr. Joseph E. Lucas, Ph.D., and John Chute, M.D., at the Duke Cancer Institute first detected this gene signature in 2007 while comparing blood-based gene expression in healthy patients to patients who had undergone full-body radiation.</span></p>
<p><span xml="lang">In 2009, Duke partnered with DxTerity and the University of Arizona to develop a high throughput radiation exposure system, a process that uses robotics and other automation to run large-scale experiments in a relatively short amount of time. The system uses a genomic testing platform from DxTerity that can use a blood sample to detect the radiation gene signature. DxTerity’s direct-from-blood test eliminates the need to first isolate RNA from the blood sample, saving time and money.</span></p>
<p><span xml="lang">“If cleared, the radiation absorption test would be the first direct-from-blood, multiplex gene expression test approved by the FDA, and would open the door for other direct-from-blood gene assays,” said Bob Terbrueggen, founder and CEO of DxTerity. The company designed the technology to allow labs around the world to run other direct-from-blood tests on existing infrastructure and at a relatively low cost.</span></p>
<p><span xml="lang">If the radiation test is cleared by the FDA, approved labs across the country would be trained to use the technology and government agencies could potentially stockpile test kits for emergencies.</span></p>
<p><span xml="lang">Duke’s</span><span lang="EN" xml="lang"> gene signature research and the DxTerity genomic testing system have other potential applications in clinical medicine. They could provide a method to evaluate </span><span xml="lang">a cancer patient’s tolerance for radiation treatment and to predict radiation-induced side effects </span><span lang="EN" xml="lang">in various types of cancers. The DxTerity platform </span><span xml="lang">is also being used to develop low-cost tests for rheumatoid arthritis and even flu detection.</span></p>
<p><span lang="EN" xml="lang">In the near future, gene expression-based testing could also spot </span><span xml="lang">early indicators of heart conditions or liver cancer.</span></p>
<p><span xml="lang">With the creation of the biodosimeter test and associated technologies, adapting it to other applications would be a matter of simply “rekeying a lock,” Phillips said. <br /></span></p>
<p><span xml="lang">The research at Duke University has been fully supported by federal funds from the Biomedical Advanced Research and Development Authority, Office of the Assistant Secretary for Preparedness and Response, Office of the Secretary, Department of Health and Human Services, under Contract No: HHSO100201000001C</span></p>
<p align="center"><span xml="lang">###</span></p>Duke MedicineTue, 17 Feb 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/gene-mutation-drives-cartilage-tumor-formation?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/gene-mutation-drives-cartilage-tumor-formation<div>DURHAM, N.C. – Duke Medicine researchers have shown how gene mutations may cause common forms of cartilage tumors.</div>
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<div><span xml="lang">In a study published in the Feb. 16, 2015, issue of the Proceedings of the National Academy of Sciences, Duke researchers and their colleagues revealed that mutations in the isocitrate dehydrogenase (IDH) gene contribute to the formation of benign tumors in cartilage that can be a precursor to malignancies. </span></div>
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<div><span xml="lang"><img align="right" border="1" height="160" hspace="1" src="http://hosting.fyleio.com/9780/public/for_ben.jpg" vspace="1" width="200" />These benign tumors, known as enchondromas, are associated with severe pain, fractures, and skeletal deformities. They also have the potential to evolve into a cancerous form known as chondrosarcomas. Over 40% of primary bone cancers are chondrosarcomas, according to the American Cancer Society. </span></div>
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<div><span xml="lang">“These findings are important for cancer treatments, as currently there are no drug therapies for enchondromas and there are no universally effective chemotherapies for chondrosarcomas,” said senior author Benjamin Alman, M.D., chair of the Orthopaedic Surgery Department at Duke University Medical Center. </span></div>
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<div><span xml="lang">All bones begin as cartilage tissue, and some of this tissue becomes growth-plate cartilage, which is responsible for bone growth. Over time, the growth-plate cells become replaced with bone. When development is complete, only the joint cartilage at the tips of the bone typically remains.</span></div>
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<div><span xml="lang">“About five percent of people have some kind of cartilage tumor in their bones, and in most cases it’s because the growth-plate cartilage cells weren’t fully replaced by bone tissue,” Alman said. “Our study sought to understand what happens to make those growth-plate cartilage cells remain, and this work will ultimately be used to determine what causes those benign tumors to become malignant.” </span></div>
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<div><span xml="lang">The researchers identified a broad range of mutations in the IDH gene in cartilage tumors. They used mice and cartilage cells in a dish to study one mutant form of IDH that is identified only in cartilage cells. They found that mutations in the IDH gene alter the way cartilage cells function during bone formation, leaving some cells behind. This is apparently what leads to enchondromas. </span></div>
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<div><span xml="lang">Previous work on cartilage tumors has been done using models based on genetic mutations that occurred only rarely in enchondromas; however, IDH mutations are present in a high percentage of enchondromas. </span></div>
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<div><span xml="lang">The researchers hope these findings will aid in developing new treatments by using animal models that more closely represent the types of mutations apparent in the vast majority of patients with enchrondromas.</span></div>
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<div><span xml="lang">For instance, the study provides evidence that drugs designed to block the function of IDH might be useful in treating benign cartilage tumors to possibly prevent their transformation to malignancy. </span></div>
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<div><span xml="lang">“By understanding what causes malignant transformation we can determine what can be done for patients with benign tumors to suppress them before they reach the malignant stage,” Alman said.</span></div>
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<div><span xml="lang">In addition to Alman, study authors at Duke include Vijitha Puviindran and Puviindran Nadesan, along with Makoto Hirata, Qingxia Wei, Shingo Sato, Yuning J. Tang, Jason Rockel, Heather Whetstone, Raymond Poon, and Angela Weng of the Hospital for Sick Children; Masato Sasaki, Rob A. Cairns, Satoshi Inoue, Wanda Y. Li, Bryan E. Snow, Tak W. Mak, and Lisa D. Jones of The Campbell Family Institute for Breast Cancer Research; Stefan Gross, Kimberly Straley, and Camelia Gliiser of Agios Pharmaceuticals; and Jay Wunder of Mount Sinai Hospital.</span></div>
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<div><span xml="lang">The National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health provided support for part of this study (R01AR066765).</span></div>
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<div><span xml="lang">IMAGE: Enchondroma-like cartilage lesions from IDH-mutant mouse models develop from aberrant cartilage cell function. Source: Duke Medicine</span></div>
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<div><span xml="lang">###</span></div>Duke MedicineMon, 16 Feb 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/newly-discovered-protein-has-link-to-gestational-diabetes?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/newly-discovered-protein-has-link-to-gestational-diabetes<p><span xml="lang">DURHAM, N.C. – </span><span xml="lang">For at least 40 years, scientists who study how the body metabolizes sugar have accepted one point: there are four enzymes that kick-start the body’s process of getting energy from food.</span></p>
<p><span xml="lang">The discovery of these four catalysts for energy production, called hexokinases, generated more research into how the body metabolizes carbohydrates, and how interfering with those enzymes through medications could help manage metabolic disorders such as diabetes.</span></p>
<p><span xml="lang">But this biochemical foursome may not deserve all of the credit. According to research by scientists at Duke and Northwestern universities, the hexokinase team actually has a fifth player. The findings appear in the online journal Nature Communications.</span></p>
<p><span xml="lang">“This swims against the past 40 years of research and what we thought we knew,” said Tim Reddy, Ph.D., a senior author of the study and assistant professor of biostatistics and bioinformatics at Duke. “Hexokinases are critical to basically all of our energy production. Finding a fifth one opens the door to more study into how we metabolize sugar, as well as genetic links to metabolic disorders.”</span></p>
<p><span xml="lang">The new protein is called HKDC1, and the researchers report that this enzyme may be a genetic predictor for whether an expectant mother develops hyperglycemia, or excess blood sugar, during pregnancy. Hyperglycemia is a potentially harmful environment for a growing fetus and can contribute to obesity and diabetes later in the child’s life.</span></p>
<p><span xml="lang">While at least 4 percent of pregnant women develop diabetes during pregnancy, as many as 400,000 women each year in the U.S. have gestational hyperglycemia, which equals about 10 percent of expectant mothers. Hyperglycemia during pregnancy may have many of the same harmful long-term health effects as full-blown gestational diabetes, according to a landmark study published in the New England Journal of Medicine in 2008.</span></p>
<p><span xml="lang">“We know that these children may be more likely to be born large and be subject to health impacts down the road, such as obesity and diabetes,” Reddy said.</span></p>
<p><span xml="lang">Doctors have counseled expectant mothers on the risks of high blood sugar and the benefits of proper diet and exercise to lessen the risk. But there currently isn’t a method to screen women for their risk of developing high blood sugar while pregnant. Often, mothers are diagnosed too late, after they have developed diabetes.</span></p>
<p><span xml="lang">While all humans have this fifth hexokinase, it appears during pregnancy, women with less of this gene are not able to metabolize glucose as well, the study showed. Researchers hope the new findings could lead to a test for pregnant women that indicates their potential for developing hyperglycemia.</span></p>
<p><span xml="lang">“The discovery of this gene creates a path forward to better predicting a woman’s risk,” Reddy said. “Knowing that there is this new hexokinase at play could also give us more information on how to inhibit or activate it, and anything we can to do disrupt the cycle would be an important advance to stem the epidemic of diabetes we see today.”</span></p>
<p><span xml="lang">Further investigation into the enzyme could create potential targets for new therapies for metabolic conditions, said William Lowe, M.D., a senior author of the study and professor of medicine at Northwestern University Feinberg School of Medicine.</span></p>
<p><span xml="lang">“This study shows the benefit of large-scale genetic studies as they begin to shed light on new molecules that are important for metabolism,” Lowe said.</span></p>
<p><span xml="lang"><span xml="lang">The idea that this enzyme has been hidden in the human genome all these years is somewhat shocking, said Christopher Newgard, Ph.D., an author of the paper and director of the Duke Molecular Physiology Institute.</span><span xml="lang"> </span></span></p>
<p><span xml="lang">“It’s ancient history in the field of carbohydrate biochemistry that there were four members of the family,” Newgard said. “Something like 40 years goes by, and then here comes this cowboy, showing up late to the party.”</span></p>
<p><span xml="lang">In addition to Reddy, Lowe and Newgard, study authors include Cong Guo; Anton E. Ludvik; Michelle E. Arlotto; M. Geoffrey Hayes; Loren L. Armstrong; Denise M. Scholtens; Christopher D. Brown; Thomas C. Becker; and Brian T. Layden.</span></p>
<p><span xml="lang">This work was funded by grants from the National Institutes of Health (T32 DK007169; DK42583; R01 MH101822) and the Department of Veterans Affairs Career Development Grant 1IK2BX001587.</span></p>
<p><span xml="lang"> </span><span xml="lang">###</span></p>Duke MedicineWed, 04 Feb 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-s-robert-califf-named-as-deputy-fda-commissioner?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-s-robert-califf-named-as-deputy-fda-commissioner<div>DURHAM, N.C. – Robert Califf, M.D., vice chancellor of clinical and translational research at Duke University School of Medicine and a global leader in cardiovascular medicine, clinical and translational research and medical economics, has been named deputy commissioner for Medical Products and Tobacco at the Food and Drug Administration. </div>
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<div><span xml="lang">Califf will begin his appointment, which was announced today by FDA Commissioner Margaret A. Hamburg, M.D., at the end of February.</span></div>
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<div><span xml="lang">“Dr. Califf has been a transformational leader at Duke for 33 years, always working to improve research and clinical care to benefit patients at Duke and around the world,” said Nancy C. Andrews, M.D., Ph.D., dean of the Duke University School of Medicine. “Recognized at Duke and among his colleagues nationally as a visionary committed to ensuring the safety and health of our global community, Dr. Califf will bring a passionate commitment to his new role with the FDA just as he has to his many roles at Duke.”</span></div>
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<div><span xml="lang">“I am delighted to accept this role with the FDA to work with its leaders and the broader government agencies to improve public health by advancing the safety and effectiveness of medical products,” Califf said. “This position will allow me the opportunity to apply the insights I have gained from my experience working for over 30 years with the many bright and dedicated people in the Duke family to help shape the future of medicine and public health.”</span></div>
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<div><span xml="lang">As deputy commissioner of the FDA, Califf will provide executive leadership to the agency’s Center for Drug Evaluation and Research, the Center for Biologics Evaluation and Research, the Center for Devices and Radiological Health, and the Center for Tobacco Products. </span></div>
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<div><span xml="lang">Califf will also oversee the Office of Special Medical Programs in the Office of the Commissioner, playing a critical role in providing high-level advice and policy direction for the federal agency’s medical product and tobacco priorities. He will also manage crosscutting clinical, scientific and regulatory initiatives in several key areas, including orphan drugs, pediatric science, and the agency’s advisory committee system.</span></div>
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<div><span xml="lang">“I am delighted to announce this important addition to FDA’s senior leadership team,” Hamburg said. “Dr. Califf’s deep knowledge and experience in the areas of medicine and clinical research will enable the agency to capitalize on, and improve upon, the significant advances we’ve made in medical product development and regulation over the last few years.” </span></div>
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<div><span xml="lang">At Duke, Califf has held many significant roles. In addition to vice chancellor of clinical and translational research, he is currently director of the Duke Translational Medicine Institute and professor of medicine in the Division of Cardiology at the Duke University School of Medicine. Califf previously served as the founding director of the Duke Clinical Research Institute, a premier academic research organization, and is one of the top 10 most-cited medical authors with over 1,200 peer-reviewed publications. </span></div>
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<div><span xml="lang">During his career, Califf has led many landmark clinical studies, and he is a nationally and internationally recognized expert in cardiovascular medicine, health outcomes research, health care quality, and clinical research. </span></div>
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<div><span xml="lang">Califf has been a pioneer in the growing field of translational research, which is key to ensuring that advances in science translate into medical care. He has also played a pivotal role in the development and leadership of the national Patient-Centered Outcomes Research Network, which is designed to enhance the quality and relevance of clinical evidence that is used to guide health decisions. </span></div>
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<div><span xml="lang">Califf was a member of the Institute of Medicine (IOM) committees that recommended Medicare coverage of clinical trials and the removal of the dietary supplement ephedra from the market, and of the IOM’s Committee on Identifying and Preventing Medication Errors. He is currently a member of the IOM Policy Committee and liaison to the Forum in Drug Discovery, Development, and Translation.</span></div>
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<div><span xml="lang">In addition, he has past experience with the FDA serving as a member of the Cardiorenal Advisory Panel and on the Science Board’s Subcommittee on Science and Technology that reviewed the FDA in 2007, producing a report entitled FDA Science and Mission at Risk.</span></div>
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<div><span xml="lang">###</span></div>Duke MedicineMon, 26 Jan 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/high-cholesterol-in-30s-40s-increases-later-risk-of-heart-disease?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/high-cholesterol-in-30s-40s-increases-later-risk-of-heart-disease<p><span style="line-height: 1.2em;">DURHAM, N.C. – Most young adults might assume they have years before needing to worry about their cholesterol.</span></p>
<p><img align="right" height="193" hspace="10" src="https://us.vocuspr.com/Publish/522300/vcsPRAsset_522300_128722_374e1345-58fa-4b01-b46a-b0cfa7151c7e_0.jpg" vspace="10" width="150" /><span>But new findings from researchers at the Duke Clinical Research Institute suggest that even slightly high cholesterol levels in otherwise healthy adults between the ages of 35 and 55 can have long-term impacts on their heart health, with every decade of high cholesterol increasing their chances of heart disease by 39 percent.</span></p>
<p><span>The findings are published in the American Heart Association journal Circulation<em>. </em>Lead author Ann Marie Navar-Boggan, M.D., Ph.D., likens the cumulative effects of elevated cholesterol to the long-term impacts of smoking.</span></p>
<p><span>“The number of years with elevated cholesterol, or ‘lipid years,’ can affect you in a similar way to the number of ‘pack years’ you have had as a smoker,” Navar-Boggan said. “It shows that what we’re doing to our blood vessels in our 20s, 30s and 40s is laying the foundation for disease that will present itself later in our lives. If we wait until our 50s or 60s to think about cardiovascular disease prevention, the cat’s already out of the bag.”</span></p>
<p><span>For the study, Navar-Boggan and colleagues at Duke, Boston University and McGill University examined data on 1,478 adults who were free of heart disease at age 55 who were part of the Framingham Heart Study, which began in 1948.</span></p>
<p><span>“Few, if any, studies have gathered the quality of the cardiovascular data that the Framingham study has," said biostatistician Michael Pencina, Ph.D., a senior author of the paper. "That wealth of data collected over time made it possible to analyze the long-term effects of cholesterol in young people—a topic on which not enough is known because it requires decades of tracking.”</span></p>
<p><span>Researchers calculated the length of time each participant had high cholesterol by age 55 and they were followed for up to 20 years to see how cholesterol levels affected their risk of heart disease.</span></p>
<p><span>Elevated cholesterol for this study was defined as non-HDL cholesterol of 160 mg/dL or higher. Researchers found similar results for patients with LDL cholesterol, or “bad cholesterol” of 130 mg/dL or higher.</span></p>
<p><span>At age 55, nearly 40 percent of participants had at least 10 years of exposure to high cholesterol. Over the next 15 years, their risk of heart disease was 16.5 percent, nearly four times the rate of 4.4 percent seen among those without high cholesterol. Each decade of high cholesterol raised the risk of heart disease by 39 percent, suggesting that the cumulative effects of even mild or moderate elevations in cholesterol pose a significant risk to heart health.</span></p>
<p><span>What was surprising, Navar-Boggan said, is that “the effect is perhaps even stronger among adults who are otherwise healthy. So even if you control everything else in your life—you don’t smoke, your blood pressure and weight are normal, and you don’t have diabetes—having elevated cholesterol over many years can still cause problems in the long run.”</span></p>
<p><span>The researchers also noted that most study participants with elevated cholesterol early in adulthood wouldn’t have met the criteria for treatment with statins, a class of medication that lowers blood cholesterol, under current guidelines endorsed by the American Heart Association and American College of Cardiology.</span></p>
<p><span>The study results suggest that otherwise healthy adults from age 35 to 55 may be a group of people who should consider cholesterol control sooner, Navar-Boggan said.</span></p>
<p><span>She cites the need for more data on the long-term effectiveness and safety of statins in younger adults.</span></p>
<p><span>The first step for young adults—a demographic known for missing regular check-ups—is to be tested.</span></p>
<p><span>“It’s never too soon for young adults to talk with their doctors about a comprehensive strategy for heart health, first and foremost focusing on diet and exercise," Navar-Boggan said. "Our study suggests, though, that young adults who cannot control cholesterol with diet and exercise alone may benefit from medication earlier in life.”</span></p>
<p><span>Study authors in addition to Navar-Boggan include Eric D. Peterson, M.D., M.P.H.; Ralph B. D’Agostino Sr., Ph.D.; Benjamin Neely, M.S.; Allan D. Sniderman, M.D.; Michael J. Pencina, Ph.D.</span></p>
<p><span>The study received funding from the Duke Clinical Research Institute and grant U19HS021092 from the Agency for Healthcare Research and Quality.</span></p>
<p><iframe allowfullscreen="" frameborder="0" height="315" src="http://corporate.dukemedicine.org//www.youtube.com/embed/p3oj3BAjkx8" width="560"></iframe></p>
<p align="center"><span>###</span></p>Duke MedicineMon, 26 Jan 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/human-mode-of-responding-to-hiv-vaccine-is-conserved-from-monkeys?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/human-mode-of-responding-to-hiv-vaccine-is-conserved-from-monkeys<div>DURHAM, N.C. – The antibody response from an HIV vaccine trial in Thailand was made possible by a genetic trait carried over in humans from an ancient ancestry with monkeys and apes, according to a study led by Duke Medicine researchers.</div>
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<div><span xml="lang">In a study published in the journal Immunity, the researchers report that an investigational vaccine that elicited an immune response in an estimated 31 percent of participants was able to do so because of a particular antibody gene motif that is shared with rhesus macaques and other primates.</span></div>
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<div><span xml="lang">When activated by the vaccine, the antibody gene makes it easy for the immune system to recognize and attack the HIV virus at a specific location on the outer coat of the virus. </span></div>
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<div><span xml="lang">The finding helps further the understanding of how the vaccine candidate, tested in Thailand in a trial known as RV144, triggered an immune response that provided modest protection. The RV144 study is the only vaccine trial to show any efficacy, so it provides data for scientists to mine. Duke researchers have played a key role in an international collaboration that has discovered many important clues into why RV144 worked and what it will take to develop a more efficacious HIV vaccine. </span></div>
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<div><span xml="lang">In their analysis, the researchers tracked the immune response in rhesus macaques that were immunized with a vaccine regimen similar to that used in the RV144 human trial in Thailand. The researchers found that the monkeys’ immune response was similar to what was seen in humans, and was actually the dominant response.</span></div>
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<div><span xml="lang">“It turns out that this antibody response that can recognize this part of the HIV envelope is encoded in the genes present throughout primate development,” said lead author Kevin Wiehe, Ph.D. “We found it in almost every primate species we studied - macaques, gorillas, bonobos and lemurs.</span></div>
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<div><span xml="lang">“When we found it in that many primate species, we then traced it back to when the common ancestor of humans and lemurs diverged - 87 million years ago. HIV has not been around that long, but other monkey retroviruses likely have, so this is an ancient antibody recognition motif that has been retained through evolution that is also used to recognize HIV.”</span></div>
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<div><span xml="lang">Wiehe and colleagues said the ancient genetic trait enables primates to produce antibodies easily to retrovirus proteins, and presents an opportunity to seek ways of boosting this ability or building upon it to create an effective vaccine.</span></div>
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<div><span xml="lang">The drawback, however, is that this specific response might compete with broadly neutralizing antibodies that can defuse the virus regardless of how it mutates.</span></div>
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<div><span xml="lang">“The place on the envelope to which antibodies were made in the RV144 trial is also a site of rare broadly neutralizing antibody binding,” said senior author Barton F. Haynes, director of the Duke Human Vaccine Institute. “What we have found is that the mode of making the non-broadly neutralizing antibodies is so dominant, that it is conserved throughout primate development over millions of years.</span></div>
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<div><span xml="lang">“Thus, our primate immune systems have been trained over many years to respond in this manner,” Haynes said. “To make broadly neutralizing antibodies, we need to bypass this remarkably highly conserved mode of antibody response to train our immune systems to respond in a new manner. That is where our current studies are focused.”</span></div>
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<div><span xml="lang">Wiehe said eliciting broadly neutralizing antibodies remains one key goal of HIV vaccine development, because the HIV virus mutates so rapidly.</span></div>
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<div><span xml="lang">“We need antibodies that can recognize multiple strains of the virus,” he said.</span></div>
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<div><span xml="lang">In addition to Haynes and Wiehe, study authors include David Easterhoff; Kan Luo; Nathan I. Nicely; Todd Bradley; Frederick H. Jaeger; S. Moses Dennison; Ruijun Zhang; Krissey E. Lloyd; Christina Stolarchuk; Robert Parks; Laura L. Sutherland; Richard M. Scearce; Lynn Morris; Jaranit Kaewkungwal; Sorachai Nitayaphan; Punnee Pitisuttithum; Supachai Rerks-Ngarm; Faruk Sinangil; Sanjay Phogat; Nelson L. Michael; Jerome H. Kim; Garnett Kelsoe; David C. Montefiori; Georgia D. Tomaras; Mattia Bonsignori; Sampa Santra; Thomas B. Kepler; S. Munir Alam; M. Anthony Moody; and Hua-Xin Liao.</span></div>
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<div><span xml="lang">The researchers received funding from the Bill &amp; Melinda Gates Foundation and the Center for HIV/AIDS Vaccine Immunology-Immuongen Discovery grant from National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health (UMI-AI100645). Additional support was provided by NIAID (5T32-AI007392, P30-AI-64518); the U.S. Army Medical Research and Material Command, the Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., and the U.S. Department of Defense.</span></div>
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<div><span xml="lang">The views expressed in the study are those of the authors and should not be construed as official or as representing the views of the Bill &amp; Melinda Gates Foundation, the Department of Defense or the Department of the Army.</span></div>
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<div><span xml="lang">###</span></div>Duke MedicineThu, 15 Jan 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/dcri-awarded-federal-contract-to-test-new-anti-infection-drugs?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/dcri-awarded-federal-contract-to-test-new-anti-infection-drugs<p>DURHAM, N.C. – The Duke Clinical Research Institute will become one of three national sites to run early clinical trials of new anti-infection therapies under a contract announced by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health.</p>
<p>The 10-year contract establishes DCRI in the Phase I Clinical Trial Units for Therapeutics, which NIAID began in 2008 to more quickly find promising therapies for diseases such as influenza, Methicillin-resistant Staphylococcus aureus (MRSA) and drug-resistant tuberculosis. </p>
<p>DCRI could launch and manage up to four early-phase clinical trials a year, and potentially receive $90 million over the life of the contract, depending on the length and complexity of the different trials.</p>
<p>“DCRI is the only academic medical center to be awarded this contract,” said principal investigator Michael Cohen-Wolkowiez, M.D., Ph.D., director of Pharmacometrics and assistant director of the Duke Pediatric Clinical Research Unit at DCRI. “We bring an outstanding operations team and unique expertise, including a state-of-the-art clinical research unit, analytical support at our pharmacometrics center, and access to healthy volunteers and patients through the medical center.”</p>
<p>Cohen-Wolkowiez said the first clinical trials at Duke will likely start later this year, after infrastructure is established. The trials will be first-in-human studies, with the goal of identifying appropriate doses prior to continuing the drug development process.<br /> <br />“We look forward to participating in this important federal effort to speed development of new drugs and therapies for infectious diseases,” Cohen-Wolkowiez said. “As these diseases are increasingly resistant to current treatments, they pose a significant public health risk and highlight the urgent need for this work.” </p>
<p align="center">###</p>Duke MedicineWed, 14 Jan 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/a-eugene-washington-m-d-to-become-dukes-next-chancellor-for-health-affairs?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/a-eugene-washington-m-d-to-become-dukes-next-chancellor-for-health-affairs<p>DURHAM, N.C. -- A. Eugene Washington, M.D., an internationally renowned clinical investigator, health-policy scholar and executive at the University of California, Los Angeles (UCLA), will become Duke University’s next chancellor for health affairs and the president and chief executive officer of the Duke University Health System, Duke President Richard H. Brodhead announced Tuesday.</p>
<p><span><img alt="Dr. A Eugene Washington" height="300" src="http://corporate.dukemedicine.org/news_and_publications/news_office/news/a-eugene-washington-m-d-to-become-dukes-next-chancellor-for-health-affairs/Washington_Dr_A_Eugene.jpeg" style="float: right; margin: 6px;" width="200" />Washington, 64, currently serves as vice chancellor for health sciences, dean of the David Geffen School of Medicine and chief executive officer of the UCLA Health System, where he is also a distinguished professor of gynecology and health policy and holds the Gerald S. Levey, M.D. Endowed Chair. At Duke, he will succeed Victor J. Dzau, M.D., who <a href="https://sites.duke.edu/medschoolblog/2014/02/19/victor-j-dzau-m-d-named-president-institute-of-medicine/">stepped down</a> as the university’s senior medical officer on June 30 to become president of the Institute of Medicine (IOM) of the National Academy of Sciences.</span></p>
<p><span>Washington has been a national leader in assessing medical technologies, translating research into health policy and shaping health care practice. He helped spearhead efforts to change clinical practice and policy guidelines for prenatal genetics, cervical cancer screening and prevention, and reproduction-related infections. He also has been a national thought leader in calling for academic health systems to reconfigure broadly and to assume the lead in creating new models for research, education, clinical care and community engagement.</span></p>
<p><span>In November, he received the David E. Rogers Award from the Association of American Medical Colleges and the Robert Wood Johnson Foundation for his “major contributions to improving the health and health care of the American people.” His work also has been recognized with the Outstanding Service Medal from the U.S. Public Health Service and election to the IOM and the American Academy of Arts and Sciences.</span></p>
<p><span>“Gene Washington has a track record of outstanding leadership in every aspect of the work of an academic medical center -- research, education and patient care,” said Brodhead. “A gifted communicator, he has special skills at getting people to work together in support of the larger mission. He has been at the forefront of the national effort to make patient outcomes the focus of health care. And he is a champion of community health who will bring that commitment to Durham. I’m delighted to have him join the Duke team.”</span></p>
<p><span>Washington was selected following a national search by a <a href="http://today.duke.edu/2014/04/medsearch">15-member Duke committee</a>. His appointment was approved by the Duke University Board of Trustees and the Duke University Health System Board of Directors.</span></p>
<p><span>“This was a comprehensive, thoughtful and inclusive search process that gave us a chance to review and meet with many outstanding candidates,” said G. Richard Wagoner Jr., immediate past chair of the Duke University Board of Trustees, who chaired the search committee. “With his deep clinical and research experience, commitment to education and demonstrated success as the head of a top-tier academic medical center, Gene Washington will lead Duke to a new level of excellence and service.”</span></p>
<p><span>Washington, who will begin his new role on April 1, will oversee one of the world’s leading academic and health care systems, including Duke’s medical school, nursing school and extensive programs for patient care, biomedical research and community service.</span></p>
<p><span>“In the world of health, this is a particularly promising time,” Washington said. “And without question, Duke is uniquely positioned among the very top health sciences institutions to take advantage of the opportunities available, given its extraordinarily accomplished people, exemplary programs across mission areas and enormously supportive partners. I feel honored and privileged to assume this key leadership role, and I look forward to working with my new colleagues to realize our full potential. Together, we will continue to build the future of science, education and health -- to the benefit of the communities and populations we serve.”</span></p>
<p><span>Prior to joining UCLA in February 2010, Washington served as executive vice chancellor and provost at the University of California, San Francisco (UCSF), where he was actively engaged in the training of medical students, residents, fellows and junior faculty, oversaw the research enterprise and steered strategic planning. He co-founded a research center that studied medical effectiveness for diverse populations and co-founded the UCSF-Stanford Evidence-based Practice Center. He also led the implementation of a UCSF diversity initiative and promoted campus-wide programs to enhance the quality of life for faculty, staff and students. Earlier at UCSF, he chaired the Department of Obstetrics, Gynecology and Reproductive Sciences for eight years. Prior to joining the UCSF faculty, Washington worked at the Centers for Disease Control and Prevention in Atlanta.</span></p>
<p><span>“I was impressed with Gene Washington’s extensive experience leading successful clinical, education and research enterprises at a health system level, and his strong commitment to excellence in all of Duke’s missions of research, education and clinical care,” said Barton F. Haynes,<strong></strong>M.D., Frederic M. Hanes Professor of Medicine, Immunology and Global Health and director of the Duke Human Vaccine Institute, who served as vice chair of the search committee. “His proven record for bringing everyone in the health system to work together will allow Duke Medicine to move to the next level of excellence and prepare well for the future.”</span></p>
<p><span>Washington, a native of Houston, said his values stem from a childhood growing up as the youngest of five children of a minister father and a mother who was a homemaker. “Growing up in Houston, I benefitted from a tremendously nurturing and supportive community and family who instilled in me the core values of excellence, integrity and service -- and these values have remained my life-long drivers,” said Washington. </span></p>
<p><span>A 1976 graduate of the UCSF School of Medicine, he completed undergraduate study at Howard University, graduate studies at both the UC Berkeley and Harvard schools of public health, and residency training at Stanford University.</span></p>
<p><span>“Gene Washington understands the challenges and opportunities that lie ahead for health and health care,” said Thomas Gorrie, chair of the Duke University Health System’s Board of Directors. “His experience, knowledge and proven leadership make him the ideal person to oversee Duke Medicine at a time of great change and innovation.”</span></p>
<p><span>Washington has served on numerous professional and government boards and committees, including the board of trustees of the Robert Wood Johnson Foundation, the scientific management review board of the National Institutes of Health, the board of directors of the California HealthCare Foundation, the editorial board of JAMA and the board of directors of The California Wellness Foundation, which he currently chairs.</span></p>
<p><span>He is the founding chair of the board of governors of the Patient-Centered Outcomes Research Institute (PCORI), a national organization authorized by the landmark 2010 Patient Protection and Affordable Care Act to advance clinical effectiveness research. PCORI recognized his significant contributions as founding chair by establishing the Eugene Washington Engagement Award, which supports active integration of patient, stakeholder and research communities during the research process.</span></p>
<p><span>Washington’s colleagues at UCLA praised his engagement and collaboration across the university.</span></p>
<p><span>“Dr. Washington has admirably served UCLA since his arrival in 2010, helping to elevate our medical enterprise to world-class status,” said UCLA Chancellor Gene Block. “He has proven himself an exceptional leader, dedicated to improving the health of citizens across the Los Angeles region and far beyond. As difficult as it is to see him go, I congratulate Dr. Washington on this tremendous new opportunity, and wish him great success in his new ventures.”</span></p>
<p><span>“Gene’s wise and extraordinarily innovative contributions to intellectual life at the Geffen School of Medicine will reverberate for years to come,” said Kelsey Martin, M.D., professor and chair of biological chemistry at UCLA and chair of UCLA Neuroscience. “He is a deep and tireless optimist who can wrestle the silver lining out of even the darkest cloud. Gene has proven that the strongest leaders combine a deep moral conviction and an unwavering commitment to excellence with genuine human warmth, compassion and humor. Duke is more than lucky to have him as their incoming chancellor.”</span></p>
<p><span>Added Judy Olian, dean of the UCLA Anderson School of Management, “Gene Washington has been a remarkable leader and a totally engaged partner across the entire university. It’s evident that his vision for the health science’s research and clinical enterprise is rooted in his fierce desire to improve the well-being of every life on this planet. The substantial advances of the health sciences under Gene have been a source of pride to all of us at UCLA.”</span></p>
<p><span>Washington and his wife Marie, who has retired from a career in finance and is active on the boards of several non-profit organizations, have been married for 32 years. They have three young adult children: a son Brooks and two daughters, Caroline and Erin.</span></p>
<p><span>“Marie and I are delighted to be joining the Durham and larger North Carolina communities, and we look forward with excitement to fostering partnerships to work to improve life across the region,” Washington said. </span></p>Duke MedicineTue, 13 Jan 2015 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-university-health-system-temporarily-restricts-hospital-visitations-2014?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/duke-university-health-system-temporarily-restricts-hospital-visitations-2014<div>
<p>Due to a rise in influenza infections throughout the Triangle, all Duke University Health System hospitals and ambulatory surgery centers will temporarily restrict patient visitations, effective Tuesday, Dec. 30.</p>
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<p>Visitors to hospital and ambulatory surgery patients will be limited to immediate family or designated caregivers age 18 and older, and who have no fever, cough or other flu-like symptoms.</p>
<p>The restrictions are part of a multi-step approach to protect patients and prevent the spread of influenza at Duke University Hospital, Duke Regional and Duke Raleigh hospitals, as well as the Duke Ambulatory Surgical Center and the James E. Davis Ambulatory Surgical Center.</p>
<p>Temporary initiatives include:</p>
<ul>
<li>Patients may receive no more than two adult visitors at one time.</li>
<li>Children under 18 are not permitted to visit hospitals or wards without prior approval from healthcare providers and only for special circumstances.</li>
<li>Visitors are urged to perform hand washing frequently, including when entering and leaving the building. Foam dispensers are available throughout the buildings, and are effective against influenza virus.</li>
<li>Visitors with fever, cough or other flu-like symptoms should remain home.</li>
<li>Emergency rooms, urgent care centers and clinics will seek opportunities to physically segregate potential flu patients if facility designs allow.</li>
</ul>
<p>Restrictions are temporary and will be reviewed as the state’s influenza rates abate. Similar restrictions on hospital visitations were put in place last year from December 30 to February 28, 2014.</p>
</div>Duke MedicineTue, 30 Dec 2014 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/researchers-map-paths-to-cancer-drug-resistance?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/researchers-map-paths-to-cancer-drug-resistance<div><span xml="lang">DURHAM, N.C. – A team of researchers led by Duke Cancer Institute has identified key events that prompt certain cancer cells to develop resistance to otherwise lethal therapies.</span></div>
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<div><span xml="lang">By mapping the specific steps that cells of melanoma, breast cancer and a blood cancer called myelofibrosis use to become resistant to drugs, the researchers now have much better targets for blocking those pathways and keeping current therapies effective. </span></div>
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<div><span xml="lang">The findings are published in two papers Dec. 23, 2014, in the journal Science Signaling.</span></div>
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<div><span xml="lang">“Clinical resistance to anticancer therapies is a major problem,” said lead author Kris Wood, Ph.D., assistant professor of Pharmacology and Cancer Biology at Duke. “The most logical way to solve the problem is to understand why tumor cells become resistant to drugs, and develop strategies to thwart these processes.</span></div>
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<div><span xml="lang">“In our studies, we developed a screening technology that allows us to quickly identify the routes cells can use to become resistant, and using that information, we were able to show that these mechanisms seen in the laboratory are actually also occurring in patients’ tumors,” Wood said.</span></div>
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<div><span xml="lang">Wood and colleagues conducted a broad survey of the known cell-signaling pathways that, when activated, have the potential to trigger resistance to drugs. Using this screening technology, they were able to corroborate the results of earlier drug-resistance studies, while also finding new pathways that had not previously been described. </span></div>
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<div><span xml="lang">The new mechanisms they identified in the laboratory were also clinically relevant, appearing in tumor cells from patients who had grown resistant to therapies. </span></div>
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<div><span xml="lang">“Interestingly, the mechanisms are quite similar among all three of the cancer types,” Wood said. “In breast cancer and melanoma, our findings suggest the same Notch-1 pathway as a potential driver of resistance to a wide array of targeted therapies -- a role that has not been widely acknowledged previously.”</span></div>
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<div><span xml="lang">Wood said that in myelofibrosis, the researchers tracked a pair of separate signaling pathways downstream of an important signaling molecule called RAS. When activated, these pathways promote resistance to current standard-of-care targeted drugs by suppressing cell death. In the second Science Signaling paper, the researchers suggest that targeting the pathways downstream of RAS may sustain the potency of current therapies. </span></div>
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<div><span xml="lang">“Together, these findings improve our ability to stratify patients into groups more and less likely to respond to therapy and design drug combinations that work together to block or delay resistance,” Wood said. </span></div>
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<div><span xml="lang">In addition to Wood, study authors on the paper entitled “Systematic identification of signaling pathways with potential to confer anticancer drug resistance” include Colin A. Martz; Kathleen A. Ottina; Katherine R. Singleton; Jeff S. Jasper; Suzanne E. Wardell; Ashley Peraza-Penton; Grace R. Anderson; Peter S. Winter; Tim Wang; Holly M. Alley; Lawrence N. Kwong; Zachary A. Cooper; Michael Tetzlaff; Pei-Ling Chen; Jeffrey C. Rathmell; Keith T. Flaherty; Jennifer A. Wargo; Donald P. McDonnell; and David M. Sabatini. </span></div>
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<div><span xml="lang">Study authors on the paper entitled “RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated aptoptosis” include Peter S. Winter; Kristopher A. Sarosiek; Kevin H. Lin; Manja Meggendorfer; Susanne Schnittger; and Anthony Letai.</span></div>
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<div><span xml="lang">The studies received funding support in part from the National Institutes of Health (CA103866, AI07389, R37DK048807, and CA129974). The manuscripts provide a full list of grant providers.</span></div>
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<div><span xml="lang">###</span></div>Duke MedicineTue, 23 Dec 2014 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/financial-toxicity-can-lower-cancer-patients-quality-of-life?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/financial-toxicity-can-lower-cancer-patients-quality-of-life<p>DURHAM, N.C. – Doctors who treat cancer are vigilant when it comes to the physical side effects of the therapies they prescribe, but financial stress from accumulating medical bills can also weigh on patients’ health — even those who have finished their treatments and are cancer-free.</p>
<p>The finding, published Dec. 16, 2014, in the Journal of Oncology Practice, advances ongoing research at Duke Medicine that has explored the issue of “financial toxicity” from cancer care and whether costs can affect a patient’s outlook and outcomes.<br /> <br />“Our focus has been on how the cost of cancer care impacts a patient’s well being, and we found that patients are at risk of experiencing financial harm as a result of the treatments we prescribe,” said Dr. Yousuf Zafar, M.D., MHS, associate professor at Duke and lead author of the study.</p>
<p>“Even for patients who have insurance, those out-of-pocket costs add up," Zafar said. "Patients are at risk for not adhering to their treatments due to cost. They may have to borrow, spend their savings, or cut back on basics like food and clothing, all to help pay for care.”</p>
<p>The findings are based on self-reported surveys and medical record data for 1,000 patients who had been diagnosed with colorectal or lung cancers at five health care systems in the U.S.; 889 of the patients were cancer-free, while 111 patients had advanced cancers. Nearly half reported difficulty making ends meet on their household income. </p>
<p>Burdensome bills can lead to what researchers call financial toxicity, and can impact patients regardless of income, employment, the status of the cancer and other health problems. A high financial burden was linked with a poorer health-related quality of life. In turn, the data also showed a relationship between patients’ quality of life and their perceptions of the quality of the care they received.</p>
<p>The study builds on previous findings that cancer patients are unlikely to discuss out-of-pocket costs with doctors, and that patients often worry that simply mentioning strained finances could result in a lower quality of care. </p>
<p>Zafar plans to continue studying interventions that might improve quality of life for financially strapped patients.</p>
<p>This and other research on financial toxicity should prompt discussion among providers on how to cut out-of-pocket costs for treatments, Zafar said. One way is to ask a pharmacist to run expensive prescriptions through patients’ insurance plans before sending the patient to the pharmacy, he said.</p>
<p>“Financial toxicity is potentially harming our patients," Zafar said. "Without a doubt, we have our patients’ best interests in mind, so if we become more cognizant of that, we’re more likely to act on it.” </p>
<p>"We as physicians don’t bear the burden of finding the answer on our own,” Zafar added. “We might not have all the answers on how to decrease our patients’ costs, but we have people around us — pharmacists, financial advisors, social workers — who are just a phone call away." </p>
<p>The research was supported with grants from the National Cancer Institute (U01 CA093344, U01 CA093332, U01 CA093329, U01 CA093324, U01 CA093348, U01 CA093339, and U01 CA093326), and by the Department of Veterans Affairs, the American Cancer Society and Duke University. A full listing of the grant support is included in the journal manuscript. </p>
<p align="center">###</p>Duke MedicineTue, 16 Dec 2014 00:00:00 +0000http://corporate.dukemedicine.org/news_and_publications/news_office/news/coffman-named-dean-designate-duke-nus-graduate-medical-school-singapore?utm_source=corporate.dukemedicine.org&utm_medium=rss&utm_campaign=RSS_news
http://corporate.dukemedicine.org/news_and_publications/news_office/news/coffman-named-dean-designate-duke-nus-graduate-medical-school-singapore<p>SINGAPORE; DURHAM, N.C. – Dr. Thomas Coffman, M.D., has been named the dean-designate at the Duke-National University of Singapore Graduate Medical School (Duke-NUS).</p>
<p>Coffman has served as executive vice-dean at Duke-NUS since Jan. 1, 2014, and will succeed Ranga Krishnan, M.D., as dean when Krishnan steps down at the conclusion of Krishnan’s term, which officially ends on June 30, 2015. Coffman is an accomplished leader and physician-scientist who has won international accolades for his work and leadership in cardiovascular medicine and kidney disease.</p>
<p>In making the announcement, Tan Chorh Chuan, president of the National University of Singapore (NUS) cited Coffman’s ability to lead Duke-NUS into its next phase of growth and development as a key pillar in Singapore’s academic medicine.</p>
<p>“We are delighted to have professor Thomas Coffman as the new Dean of Duke-NUS,” Tan said. “Professor Coffman has been working closely with Dean Ranga Krishnan and the Duke-NUS leadership team on many of the key initiatives developed by the school this year. Professor Coffman is a distinguished clinician-scientist and academic leader, and I am confident that he will build further on the outstanding achievements made by Dean Krishnan, and bring Duke-NUS to the next level of global excellence.” </p>
<p>“These are big shoes to fill,” Coffman said. “As dean-designate of Duke-NUS, I hope to build on the strong foundation laid by Dean Sandy Williams and Dean Ranga Krishnan. Duke-NUS will continue to be a pre-eminent leader in the region for the training of clinicians, clinician-scientists and researchers, and the conduct of translational, clinical and basic research. I look forward to working with the ministries within Singapore, as well as colleagues at the school and in the community, to continue to advance the school’s mission.”</p>
<p> </p>
<p>Coffman came to Duke in 1980 for his internship, and he stayed through residency, fellowship training and as a faculty member and institutional leader at Duke, the Durham Veterans Affairs Medical Center, and Duke-NUS.</p>
<p>Among his accomplishments, Coffman is a recognized national and international leader in nephrology. He served as president of the American Society of Nephrology in 2008-2009. In 2012, a Duke team led by Coffman was awarded a five-year, $5.8 million grant from the National Institute of Diabetes and Digestive and Kidney Diseases to create the Duke O’Brien Center for Kidney Research. He will maintain his academic appointment in the Department of Medicine. </p>
<p>“Tom has been instrumental in the success of Duke-NUS over the past few years as executive vice dean and program director of the Signature Research Program in Cardiovascular and Metabolic Disorders,” said Michael Merson, M.D., vice chancellor for Duke-NUS Affairs and a member of the Duke-NUS Governing Board. “He has a clear vision of the future for Duke-NUS which includes continuing to be an agent of change in the practice of medicine and enhancing the already excellent partnership with SingHealth in the new academic medical center.”</p>
<p>Duke and the NUS signed a formal agreement in April 2005 under which the two institutions would establish a new medical school in Singapore. Under the agreement, the Singapore government made a significant investment to establish Duke-NUS as part of Singapore’s strategy to become a leading center for medical research and education. It has more recently established an Academic Medical Center partnership with SingHealth. The school's curriculum is patterned after that of the Duke University School of Medicine, and is part of the National University of Singapore system. To date the school has graduated a total of 158 M.D and three Ph.D. students.</p>
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